Patients with kidney disease, particularly those with end stage renal disease (ESRD), require hemodialysis in order to remove metabolites and the like from their blood stream. This can be a very time-consuming process, but the time can be lessened by providing a large blood flow to the hemodialysis machine. Even though this is done, hemodialysis can still take about four hours and is needed about three times a week.
In order to provide high blood flow to and from the hemodialysis machine, vascular access with high blood flow is needed. One method of providing this is illustrated in FIG. 1. An artery 10 and a vein 12 are located in the arm 14 of the patient. A vessel 16, known as an AV graft or shunt, is grafted to connect the artery 10 and the vein 12. As the AV graft 16 is a direct connection between the artery 10 and the vein 12 and has a relatively large cross-sectional area, a high flow through it occurs. The direction of flow is indicated by the arrows in FIG. 1. Catheters (not shown) can be connected to the AV graft 16, when hemodialysis is required. The catheters can tap into the high flow through the AV graft 16 to provide a high flow to and from the hemodialysis machine.
However, there are also considerable problems with this technique. One of these, illustrated in FIG. 2, is that stenosis 18 occurs at the outflow tract where the AV graft 16 is connected to the vein 12, that is at the venous anastomosis side of the graft. The stenosis 18 is an unnatural narrowing of the vessel, and if unopened by angioplasty, the stenosis 18 progresses until the vein 12 is completely blocked. The stenosis 18 is due to neo-intimal hyperplasia, that is the response of the vessel 16 to the abnormal conditions.
Various mechanisms are considered as possibly contributing to the development of the stenosis 18. The flow through the vein 12 is typically 10 to 20 times higher than normal. This leads to turbulence and flow separation such that the flow is not smooth or laminar, and the stenosis 18 develops as a result. Another factor is that the vein 12 is exposed to a higher blood pressure than normal, because it is directly connected to the artery 10. The blood pressure in an artery 10 is typically 100 mm Hg, whereas the blood pressure in a vein 12 is typically 5 mm Hg. The vein 12 tends to arterialize in response to this, for example by thickening of the vein wall and this may contribute to the stenosis 18. A further possible factor is that, in the presence of the graft, the flow in the vein 12 is pulsatile. There is a significant compliance mismatch between the AV graft 16, which, if synthetic, is quasi-rigid, and the vein 12 which is compliant. The pulsatile flow produces an oscillating stress concentration at the junction, i.e. suture line, between the AV graft 16 and the vein 12. Although the suture usually does not fail, the stenosis 18 may be in response to the oscillating stress concentrated at the junction.
This is a considerable problem. In 90% of AV grafts (e.g., AV graft 16), stenosis 18 develops at the venous anastomosis side. AV graft survival is around only 1.5 years. Conventionally, alleviation of this problem requires surgery, such as angioplasty to remove the stenosis 18 or surgery to implant a new AV graft in a different limb of the patient.
A further problem is that the AV graft 16 effectively provides a short circuit between the artery 10 and the vein 12 and the high flow through the AV graft 16 requires a huge additional cardiac output. Normal cardiac output is typically 5 liters per minute, but with the AV graft 16 in place this can increase to 7 liters per minute. This large additional cardiac output can be very problematic indeed, and can result in fatal cardiac failure for about 5% of AV graft patients.